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Oxygen poisoning in mice. Ultrastructural and surfactant studies during exposure and recovery.

I Y Adamson, +2 more
- 01 Nov 1970 - 
- Vol. 90, Iss: 5, pp 463-472
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This article is published in Archives of pathology.The article was published on 1970-11-01 and is currently open access. It has received 82 citations till now. The article focuses on the topics: Pulmonary surfactant & Histocytochemistry.

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Metabolic activation and biological effects of nitrosamines in the mammalian lung.

TL;DR: Evidence in vitro suggests selective uptake of nitrosamine by cell type-specific receptors, a phenomenon which offers a more logical explanation than previously published theories for the selectivity of biological effects exerted by nitrosamines.
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A new model of diffuse interstitial pulmonary fibrosis in the rat

TL;DR: It is concluded that lung damage produced by the combination of low doses of paraquat plus normobaric 74% O2 concentration in the breathing air is an adequate experimental model of diffuse interstitial pulmonary fibrosis as it occurs in many of the human cases of this condition.
Journal ArticleDOI

Alveolar Epithelial Dynamics in Postpneumonectomy Lung Growth

TL;DR: The data suggest an active contribution of localAlveolar Type II cells to alveolar growth, and the active transcription of angiogenesis‐related genes both before and after pneumonectomy.
Journal ArticleDOI

Epithelial ablation of Bcl-XL increases sensitivity to oxygen without disrupting lung development.

TL;DR: Findings reveal that the epithelial-specific expression of Bcl-X(L) is not required for proper lung development, but functions to protect respiratory epithelial cells against oxygen-induced toxicity, such as during hyperoxia and the lung's first exposure to ambient air.
Journal ArticleDOI

Oxygen-induced lung toxicity: Effect on serotonin disposition and metabolism

TL;DR: It was shown that lung levels of 5-HT and [ 3 H]5-HT correlated with the degree of oxygen-induced injury to the pulmonary vasculature and suggested that 5- HT may be a factor in the pathogenesis of the vasculatures injury and/or pulmonary edema formation.
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